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Abdominal surgeries have high rates of surgical site infections (SSIs), contributing to increased morbidity and mortality and costs for hospitalization. The aim of this study was to determine the SSI incidence rates and risk factors after abdominal surgeries.This prospective cohort study included all patients undergoing abdominal surgeries between 2005 and 2007 in the Western Galilee Medical Center in Nahariya, Israel. SSI incidence rates were calculated per 100 operations. Odds ratios (ORs) were estimated for each risk factor using univariate and multivariate analyses by logistic regression models.Among 302 patients in the study cohort, the total SSI incidence rate was 22.2%. The univariate analysis defined 13 variables significantly associated with SSI: age60 years, lower functional status, diabetes mellitus, congestive heart failure, immunocompromising underlying disease, treatment with chemotherapy and other immunosuppressive medications, impaired immune system open cholecystectomy, laparotomy, an American Society of Anesthesiologists (ASA) score2, drain insertion, and 'dirty wound' classification. In multivariate regression analysis, treatment with immunosuppressive medications (OR = 2.5, 95% confidence interval (CI) = 1.099-143.443), open cholecystectomy (OR = 2.25, 95% CI = 2.242-40.109), and dirty wound classification (OR = 2.179, 95% CI = 3.80-20.551) were significantly associated with SSI.The significant risk factors defined should be addressed preoperatively to decrease the risk for SSI. Wound surveillance in the post-discharge period is necessary for correct estimation of SSI rates.

We report three female patients suffering from toxic epidermal necrolysis, with 30% to 70% epidermal detachment. Alleged causative agents were dipyrone, dibenzazepine, and allopurinol. All patients were treated by intravenous immunoglobulins (IVIG) and survived without further complications, although poor prognostic factors such as concomitant diabetes, large areas of epidermal detachment, and pancytopenia were present. We report these cases with emphasis on the concept that prompt diagnosis, withdrawal of causative drugs, and immediate treatment are imperative for the favorable outcome of the disease. Our patients can be added to the list of those patients who were successfully treated by IVIG, as indicated in this review of the literature.

In this unusual case, we report the history of a patient who was hospitalized with pulmonary manifestations presenting as broncholitis obliterance organizing pneumonia (BOOP) associated with ANCA-negative pauci-immune glomerulonephritis. Other known causes for the occurrence of BOOP were excluded. Immediate diagnosis and treatment with a combination of steroids and cytotoxic therapy resulted in a complete remission and prevented eventual dialysis.

Induction of enhanced anticryptococcal activity in human monocyte-derived macrophages (HMM) by macrophage colony-stimulating factor (M-CSF) and possible synergy with fluconazole (FCZ) for killing of Cryptococcus neoformans (CN) was studied. Fungistasis by HMM cultured in medium for 3, 5, or 7 days was minimal, 0-17%. The fungistasis of HMM cocultured with M-CSF at 1000, 5000, or 20,000 U/ml for 3, 5, or 7 days was increased significantly (P0.02) at all study times and by all concentrations. The optimal M-CSF concentration for HMM treatment for enhanced fungistasis was 5000 U/ml for Day 3 (84%), whereas 1000 U/ml was sufficient with more prolonged HMM culture and M-CSF treatment (Days 5-7). The enhancement by M-CSF was seen with four different donors and three patient isolates of CN. FCZ at 5 micrograms/ml was fungicidal, 28 +/- 17% (n = 8). Killing by FCZ was enhanced by HMM treated with M-CSF 5000 or 20,000 U/ml for 5 days compared to control HMM, 58% (P = 0.001) and 60% (P = 0.002) vs 48%, respectively. This was also seen with HMM cultured with 1000 U/ml M-CSF for 7 days (P0.05). M-CSF also induced in HMM enhancement of fungistasis by lower, fungistatic, concentrations of FCZ. These results demonstrate enhancement of anticryptococcal activity by HMM treated with M-CSF and synergy with FCZ for inhibition and killing. These findings may provide a rationale for combined treatment of FCZ and M-CSF against cryptococcosis.

The anticryptococcal activity of murine bronchoalveolar macrophages (BAM) and their synergy with fluconazole (FCZ) was studied. BAM cultured with tissue culture medium for 48 to 72 h were fungicidal (24 to 39%) in a 3-h killing assay. However, net killing of Cryptococcus neoformans did not continue when culture time was extended to 24 h, although BAM were fungistatic (88 to 98%). Treatment with macrophage colony-stimulating factor (M-CSF; 5,000 U/ml, 48 h) did not significantly increase BAM killing of a low challenge dose in 3-h assays compared with control BAM. However, M-CSF-treated BAM were significantly more fungistatic against higher challenge doses in the 3-h assays. FCZ was not fungicidal at 5 micrograms/ml but was highly fungistatic (98 and 99% at 24 and 48 h, respectively). M-CSF-treated BAM acted synergistically with FCZ (2.5 micrograms/ml) for significantly greater killing than control BAM, 55% versus 20% and 96% versus 45% at 24 h and 48 h, respectively. Killing by M-CSF BAM and FCZ (5.0 micrograms/ml) was significantly (P < 0.01) greater than that by control BAM and FCZ at 48 h. These findings indicate an important collaborative role for BAM and FCZ in killing C. neoformans, and this is enhanced by M-CSF.

Particular systemic infections have been found to be associated with concurrent malignancies sufficiently commonly as to warrant search for malignancy in patients with such infections. The current study adds Streptococcus pneumonia endocarditis to the list of relevant infections.

Primary effusion lymphoma (PEL) is a unique clinicopathological entity associated with human herpesvirus-8 (HHV-8) infection, occurring almost exclusively in human immunodeficiency virus (HIV)-infected individuals. We report a rare case of HHV-8-negative PEL in an HIV-negative elderly patient who presented with pleural effusion. The patient was treated with CHOP and Rituximab. As opposed to the general poor outcome of this disease, our patient achieved complete remission and is still without signs of disease 11 months after the last treatment.

Candida albicans and C. dubliniensis genotype differences among Israeli ethnic groups were assessed. Isolates from Jews (51), Arabs (35) and Druze (25) were genotyped. The distributions among ethnic groups were not different, however they differed (p = 0.002) from global populations. Therefore, C. albicans and C. dubliniensis genotype distribution differences in Israel are related to changes in all ethnic groups.

Intravesicular instillation of bacille Calmette–Guerin (BCG), an attenuated variant of the virulent strain of Mycobacterium bovis, has been extensively used as the treatment of choice for bladder cancer since first approved in 1976. Adverse effects of treatment are rare and mostly local, with systemic reactions complicating up to 5% of patients. The majority of serious side effects have occurred in immunocompromised patients. Even more rare is bone marrow involvement. Only two previous cases are reported in the medical English literature; in these cases, the granulomas were non-caseating. We describe a patient who developed fever and pancytopenia associated with mycobacterial infection after intravesicular instillation of BCG. Caseating granulomas were seen in the bone marrow biopsy and, later, bone marrow fibrosis developed gradually, in spite of successful treatment with antimycobacterial agents.

Macrophage colony-stimulating factor (M-CSF) given subcutaneously at a dose of 2.5 mg/kg of body weight (4.75 x 10(6) U/kg) to CD-1 male mice 8 to 12 weeks old was found to enhance significantly the fungistasis of bronchoalveolar macrophages (BAM) against Cryptococcus neoformans. When M-CSF was given 1, 3, 7, 9, or 13 days before an ex vivo challenge with C. neoformans, fungistasis was increased (P ranged from < 0.05 to < 0.001) compared with that induced by control BAM. A maximum effect was seen by days 1 and 3 after administration of M-CSF. Twenty-one days after M-CSF, BAM did not produce significantly enhanced fungistasis. M-CSF also significantly enhances the fungistatic effect of peritoneal macrophages (PM) if given 1, 3, and 7 days prior to testing against C. neoformans in comparison with control PM (P ranged from < 0.05 to < 0.001). PM did not produce enhanced fungistasis 9 or 13 days after administration of M-CSF. These studies demonstrating in vivo enhancement of anticryptococcal activity of macrophages with M-CSF provide a rationale for in vivo use of M-CSF to enhance resistance to infection with C. neoformans.

Of the six known species of Listeria, Listeria monocytogenes is classified as the only human pathogen causing listeriosis, a highly fatal, opportunistic infection contracted via food. Listeria ivanovii is the only other pathogenic species of the genus and is considered to be specific to ruminants, except for extremely rare cases of infection in humans. We report here on a 64-year-old male patient with L. ivanovii who responded favorably to treatment with intravenous ampicillin.

Endocarditis is a rare complication of salmonellosis. The most frequently observed species is Salmonella typhi. Endocarditis caused by Salmonella paratyphi is extremely rare with only three previous cases documented in the medical literature. We report a case of endocarditis caused by Salmonella paratyphi in an otherwise healthy young patient, with full recovery after appropriate antibiotic treatment.

The inhibitory effect of human serum on the multiplication of Cryptococcus neoformans and the interaction with fluconazole were studied. Compared with cryptococcal multiplication in RPMI 1640 medium alone, 5% human serum in medium inhibited multiplication by 76% +/- 6% (n = 8). The inhibitory effect of human serum was donor independent, [corrected] heat stable (56 degrees C, 30 min), and not due to albumin or globulin. Bovine and murine sera were not inhibitory at that concentration. A fungistatic concentration of fluconazole (5.0 micrograms/ml) in medium plus 5% human serum resulted in 40% +/- 5% (n = 8) killing (reduction of inoculum CFU) in a 24-h assay. Bovine or murine sera did not have the enhancing effect, and this human serum activity was heat stable and donor independent. At 2.5 micrograms of fluconazole per ml, fungistasis by fluconazole plus human serum was significantly greater than with either alone. Higher serum concentrations [corrected] potentiated fluconazole more. At higher fluconazole concentrations (e.g., 20 micrograms/ml) fluconazole alone could kill, but serum potentiated this. A fluconazole-resistant isolate (MIC, 100 micrograms/ml) was not killed by fluconazole (5.0 micrograms/ml) in 5% human serum, but human serum potentiated the partial fluconazole inhibition. When human serum was dialyzed (molecular weight cutoff, 6,000 to 8,000) against phosphate-buffered saline, it lost the ability to synergize with fluconazole for killing Cryptococcus organisms but not the capacity to inhibit multiplication. Filtration of serum suggested the filtrate with a molecular weight of < 10,000 could interact synergistically with fluconazole for killing but could not inhibit cryptococcal multiplication. These findings indicate that human serum has two components, one (macromolecular) with a unique ability to inhibit C. neoformans and a low-molecular-weight component that enhances fluconazole anticryptococcal activity.

The interaction of human macrophages with the yeast-form of Histoplasma capsulatum was studied. The use of culture and a short-term assay period instead of microscopy gave direct evidence of the fungicidal activity of human macrophages. The present study reports the novel finding of fungicidal activity of macrophages derived from monocytes in the presence of macrophage colony-stimulating-factor (MCSF). The induction of fungicidal activity by this cytokine was dose dependent. MCSF at 10,000 U/ml was optimal with 73(SD3)% killing. Inhibition of macrophage killing by superoxide dismutase (SOD), but not catalase (CAT) or N-monomethyl-L-arginine (NMMA), established the role of the superoxide anion in the killing mechanism. The fungistatic activity of MCSF-derived human macrophages in a 24-h assay was also dose dependent and was not inhibited by SOD, CAT or NMMA. MCSF at 10,000 U/ml produced optimal macrophage fungistatic activity, 34.6(SD4)%.

The clinical implications of non-alcoholic fatty liver diseases (NAFLD) derive from their potential to progress to fibrosis and cirrhosis. Inappropriate dietary fat intake, excessive intake of soft drinks, insulin resistance and increased oxidative stress results in increased free fatty acid delivery to the liver and increased hepatic triglyceride (TG) accumulation. An olive oil-rich diet decreases accumulation of TGs in the liver, improves postprandial TGs, glucose and glucagon-like peptide-1 responses in insulin-resistant subjects, and upregulates glucose transporter-2 expression in the liver. The principal mechanisms include: decreased nuclear factor-kappaB activation, decreased low-density lipoprotein oxidation, and improved insulin resistance by reduced production of inflammatory cytokines (tumor necrosis factor, interleukin-6) and improvement of jun N-terminal kinase-mediated phosphorylation of insulin receptor substrate-1. The beneficial effect of the Mediterranean diet is derived from monounsaturated fatty acids, mainly from olive oil. In this review, we describe the dietary sources of the monounsaturated fatty acids, the composition of olive oil, dietary fats and their relationship to insulin resistance and postprandial lipid and glucose responses in non-alcoholic steatohepatitis, clinical and experimental studies that assess the relationship between olive oil and NAFLD, and the mechanism by which olive oil ameliorates fatty liver, and we discuss future perspectives.

Background In previous open-label noncomparative clinical trials, both fluconazole and itraconazole were effective therapy for progressive forms of coccidioidomycosis. Objective To determine whether fluconazole or itraconazole is superior for treatment of nonmeningeal progressive coccidioidal infections. Design Randomized, double-blind, placebo-controlled trial. Setting 7 treatment centers in California, Arizona, and Texas. Patients 198 patients with chronic pulmonary, soft tissue, or skeletal coccidioidal infections. Intervention Oral fluconazole, 400 mg/d, or itraconazole, 200 mg twice daily. Measurements After 4, 8, and 12 months, a predefined scoring system was used to assess severity of infection. Findings were compared with those at baseline. Results Overall, 50% of patients (47 of 94) and 63% of patients (61 of 97) responded to 8 months of treatment with fluconazole and itraconazole, respectively (difference, 13 percentage points [95% CI, -2 to 28 percentage points]; P = 0.08). Patients with skeletal infections responded twice as frequently to itraconazole as to fluconazole. By 12 months, 57% of patients had responded to fluconazole and 72% had responded to itraconazole (difference, 15 percentage points [CI, 0.003 to 30 percentage points]; P = 0.05). Soft tissue disease was associated with increased likelihood of response, as in previous studies. Azole drug was detected in serum specimens from all but 3 patients; however, drug concentrations were not helpful in predicting outcome. Relapse rates after discontinuation of therapy did not differ significantly between groups (28% after fluconazole treatment and 18% after itraconazole treatment). Both drugs were well tolerated. Conclusions Neither fluconazole nor itraconazole showed statistically superior efficacy in nonmeningeal coccidioidomycosis, although there is a trend toward slightly greater efficacy with itraconazole at the doses studied.